Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of agonists and antagonists of GABA-ergic system on analgesia induced by clonidine was investigated in the rat. The compounds activating (muscimol, 1 mg/kg and aminooxyacetic acid; AOAA, 25 mg/kg) or inhibiting GABA-ergic receptors (bicuculline and picrotoxin, in subconvulsive doses 0.5-1 mg/kg) do not change clonidine-induced analgesia. Only the higher dose (2 mg/kg) of muscimol, bicuculline or picrotoxin affected clonidine-induced analgesia. Baclofen, contrary to other GABA agonists, markedly potentiated clonidine-induced analgesia in the dose dependent manner. These results suggest that compounds activating and inhibiting GABA A receptors (muscimol, AOAA, bicuculline and picrotoxin) have a weak influence on clonidine induced analgesia as compared to the effect of baclofen (agonist of GABA B receptors).
 ...
PMID:The influence of GABA-ergic system on clonidine analgesia in rats. 789 27

It has been demonstrated that electroacupuncture (EA) produces analgesia in acute arthritic animal models, while the differential analgesic effects at different EA parameters remains to be discovered. In the present experiment, the effects of EA at 100 Hz and 15 Hz on bilateral Yanglingpuan acupoints of the arthritic rats was studied. The results showed: 1) 15Hz EA was more effective than 10Hz EA for analgesia; 2) spinal glutamic acid content of the 15-Hz EA group was significantly lower than that of the 100-Hz EA group, and 3) no significant difference in GABA contents between the two groups was found. The results suggest that spinal glutamic acid may be involved in the different analgesic effects of EA at different frequencies in arthritic rats.
 ...
PMID:[Effects of electroacupuncture at different frequencies on the nociceptive response and central contents of GABA and glutamic acid in arthritic rats]. 791 73

The dorsal raphe nucleus (DRN) is an important nucleus in pain modulation. It has abundant 5-HT neurons and many other neurotransmitter and/or neuromodulator containing neurons. Its vast fiber connections to other parts of the central nervous system provide a morphological basis for its pain modulating function. Its descending projections, via the nucleus raphe magnus or directly, modulate the responses caused by noxious stimulation of the spinal dorsal horn neurons. In ascending projections, it directly modulates the responses of pain sensitive neurons in the thalamus. It can also be involved in analgesia effects induced by the arcuate nucleus of the hypothalamus. Neurophysiologic and neuropharmacologic results suggest that 5-HT neurons and ENKergic neurons in the DRN are pain inhibitory, and GABA neurons are the opposite. The studies of the intrinsic synapses between ENKergic neurons, GABAergic neurons, and 5-HT neurons within the DRN throw light on their relations in pain modulation functions, and further explain their functions in pain mediation.
 ...
PMID:The dorsal raphe: an important nucleus in pain modulation. 792 1

The intrathecal (IT) injection of progesterone (PROG) or three of its ring A-reduced metabolites (5 beta,3 alpha-pregnanolone, 5 alpha,3 alpha-pregnanolone, or 5 beta,3 beta-pregnanolone) did not significantly alter any of two pain thresholds (vocalization threshold to tail shock, VTTS, or tail flick latency, TFL) in ovariectomized rats when tested in a wide range of doses (2.5-250 micrograms). When combined with a subanalgesic dose of muscimol (MUSC; 1 microgram IT), PROG and its two 3 alpha-hydroxy derivatives, but not the 3 beta, caused significant analgesia in the VTTS but not in the TFL test. No clear dose-response relationships were noted in the analgesic response to the combination of the progestins and MUSC. The present results indicate that PROG, either directly or through its ring A-reduction, can modulate nociceptive information by enhancing the action of GABA agonists on GABAA receptors.
 ...
PMID:Perispinal progestins enhance the antinociceptive effects of muscimol in the rat. 811 19

Current pharmacotherapeutic approaches to the management of violent and aggressive behavior rely mostly on agents that act as receptor agonists or antagonists at subtypes of brain dopaminergic, GABAergic, and serotonergic receptors. Ethological experimental studies in animals have shown that drugs may modulate aggression by inhibiting motor activity, by distorting aggression-provoking or -inhibiting signals, by fragmenting behavioral sequences or temporal patterning, or by increasing the rate and intensity of aggressive acts. Evidence from animal studies points to large changes in selected brain dopamine, serotonin, and GABA systems during and following aggressive and defensive behavior. However, the specificity of drugs that are currently used to control aggressive behavior through their action as agonists or antagonists at subtypes of dopamine, serotonin or GABA receptors continues to be of concern. Similar to the effects of widely used traditional neuroleptics that nonselectively antagonize dopamine receptors, the range of behaviors which is suppressed by either D1 or D2 receptor antagonists is pervasive. At present, systemic administration of dopamine receptor antagonists in animal preparations does not target aggression-specific mechanisms. The GABAA/Benzodiazepine/Chloride ionophore receptor complex is implicated in the aggression-heightening effects of alcohol and benzodiazepines. Although early reports focused on the "taming" effects of benzodiazepine anxiolytics, low doses may enhance aggression in both animals and humans. Benzodiazepine antagonists block heightened aggression after low doses of alcohol or benzodiazepines. Agonists at certain 5-HT1 receptor subtypes such as eltoprazine are potently effective in reducing aggressive behavior of males and females of various animal species under conditions that promote charging offensive-type aggression, without adversely affecting nonaggressive components of the behavioral repertoire. However, recent reports indicate that eltoprazine and related compounds may potentiate anxiety reactions in rodents, and question the behavioral specificity of these substances. Opioid receptor antagonists modulate primarily physiological and behavioral responses of defense and submission. Defeated animals show tolerance to opiate analgesia and withdrawal responses upon challenge with opioid receptor antagonists. Defensive and submissive vocalizations are potently blocked by opioid peptides. Substances that target specific receptor subtypes at serotonergic, GABAergic and opioidergic synapses are most promising for the selective modification of aggressive, defensive and submissive behavior patterns.
 ...
PMID:Neurobiological mechanisms controlling aggression: preclinical developments for pharmacotherapeutic interventions. 817 Jun 25

Based on pharmacological evidence that inhibitory amino acids mediate vaginocervical mechano-stimulation produced analgesia (VSPA), we hypothesized that inhibitory amino acids would be released endogenously in the spinal cord in response to vaginocervical mechano-stimulation (VS). This hypothesis was tested by HPLC analysis of the amino acid content of 5-min superfusates of the spinal cord before, during and after VS (400 g force applied against the cervix) in urethane-anesthetized rats. Utilizing an in vivo push-pull superfusion method, artificial cerebrospinal fluid was continuously superfused over the spinal cord through the intrathecal space surrounding the sacral-lower thoracic region. In addition, concentrations of amino acids in the superfusate were measured in response to KCl stimulation (increasing the superfusion medium from 3.4 to 40.0 mM KCl to produce non-specific depolarization), and noxious hind paw mechano-stimulation (pinching the hind paw to produce a sustained flexor response in ipsilateral hind leg). There was a significant increase in the concentration of Gly, Tau, Asp, Glu and Lys in the superfusate in response to VS (n = 8) and to KCl (n = 8), but not to hind paw stimulation (n = 5). Also, GABA concentrations increased in response to KCl, and the concentration of Ala, Ser, Gln, Thr, Arg and Phe increased in response to VS, however, GABA levels were sometimes below the limits of detection. In contrast, there was no significant change in any amino acid concentration in response to hind paw pinch stimulation, and VS did not significantly affect the concentrations of Tyr, His, Ile, Leu, Met, Trp or Val. The present findings support our hypothesis that VS releases inhibitory amino acids in the spinal cord. Moreover, other amino acids, including 'excitatory' amino acids, are released into the superfusate. The profile of amino acid release in response to VS differs from that in response to paw pinch or KCl administration.
 ...
PMID:Release of amino acids into regional superfusates of the spinal cord by mechano-stimulation of the reproductive tract. 824 40

The present study was designed to characterise the analgesia produced by the GABA B agonist baclofen in tonic pain in monkeys. The effect of various doses of baclofen was studied on formalin induced pain. Baclofen was injected intraperitoneally 30 min prior to formalin injection in five doses of 2, 4, 6, 8, and 10 mg/kg and the pain was quantified for a period of one hour. Baclofen produced dose related analgesia, 6 mg/kg having maximal effect. The antinociceptive effect of baclofen could be attributed to the effect of baclofen on GABA B receptors producing presynaptic inhibition of primary nociceptive afferents in the dorsal horn of the spinal cord.
 ...
PMID:GABA B mediated analgesia in tonic pain in monkeys. 827 93

In order to determine whether or not neuropeptide Y coexists with GABA or glycine in rat dorsal horn, we have examined 84 neuropeptide Y-immunoreactive neurons in laminae I-III with a combined pre- and postembedding immunocytochemical method. All of the neuropeptide Y-immuno-reactive neurons were also GABA-immunoreactive, but they were either non-immunoreactive or weakly immunoreactive with the glycine antiserum. In addition, a double-label immunofluorescence method was used to search for co-localization of neuropeptide Y and [Met]enkephalin in spinal cord. Although the two types of peptide immunoreactivity often coexisted in varicosities around the central canal and in the ventral horn, such coexistence was not seen in the superficial dorsal horn. These results suggest that neuropeptide Y is present in GABAergic neurons in laminae I-III of rat dorsal horn, but that it is largely or completely restricted to those neurons which do not contain glycine. In addition, the cells that contain GABA and neuropeptide Y appear to form a different population from those that contain GABA and [Met]enkephalin. Neuropeptide Y administered by intrathecal injection causes analgesia, and there is evidence that this may involve a presynaptic mechanism. The results of the present study suggest that neuropeptide Y may act in conjunction with GABA to produce presynaptic inhibition of nociceptive primary afferents.
 ...
PMID:Evidence that neuropeptide Y is present in GABAergic neurons in the superficial dorsal horn of the rat spinal cord. 849 14

The purpose of this study was to verify the role of somatostatin (Som) of brain in analgesia of electroacupuncture (EA). Intracerebroventricular (icv) injection of Som caused a more marked elevation of pain threshold and of EA analgesic effect, but the activity of Ca(2+)-APTase in hippocampus was significantly decreased; The Som and GABA levels in hippocampus and brain stem were decreased by EA analgesia. The Som in hippocampus and brain stem were obviously depleted by icv injection of cycteamine, but without any change of pain threshold and analgesic effect of EA. These results indicated that the exogenous Som of brain potentiated the analgesic effect of EA, however, the decrease of endogenous of some brain regions took part in the process of EA analgesia.
 ...
PMID:[Effect of brain somatostatin on electroacupuncture analgesia of rat]. 875 23

The influence of GABA agonists and antagonists on analgesic activity of imipramine (IMA, 20 mg/kg, ip) was studied using the hotplate method. Administration of GABAA receptor agonist muscimol (1 mg/kg, ip), GABAB receptor agonist baclofen (3 mg/kg, ip) or GABA-T inhibitor aminooxyacetic acid (25 mg/kg, ip) increased the analgesic effect of IMA. On the other hand pretreatment of GABAA receptor antagonist bicucukline (2 mg/kg ip), GABAB receptor antagonist delta-amino-n-valeric acid (50 mg/kg, ip) or GABA synthesis inhibitor thiosemicarbazide (50 mg/kg, ip) attenuated the IMA analgesia. These results suggest that the analgesic action of IMA may be mediated by functional alteration of a central GABAergic mechanism and/or subsequent stimulation of GABA receptors.
 ...
PMID:GABAergic agents modify imipramine analgesia. 886 80


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>